Our findings suggest that resveratrol reduces cytosolic [Ca] and SR [Ca] in ASMCs in normal physiological saline, which might be, at least in part, mediated by the NCX.Cerebral ischemia-reperfusion (I/R) injury is a terrible disease which results in the dysfunction and structural damage of brain tissues. Growing evidence implies that miR-455-5p is implicated in the regulation of pathogenesis of several diseases. The aim of this study is to reveal the role of miR-455-5p in cerebral I/R injury and the regulatory mechanism. We established a vitro model by inducing SH-SY5Y and PC-12 cells with oxygen-glucose deprivation and reoxygenation. The experimental cerebral I/R rat model was established by middle cerebral artery occlusion operation. The findings indicated that miR-455-5p expression was downregulated in oxygen-glucose deprivation and reoxygenation induced cells and I/R rat model. In addition, miR-455-5p upregulation inhibited SH-SY5Y cell apoptosis and cerebral damage, whereas miR-455-5p silencing promoted SH-SY5Y cell apoptosis and cerebral damage. Mechanistically, luciferase reporter assay corroborated that miR-455-5p could bind with feline mcDonough sarcoma-like tyrosine kinase 3 (FLT3) mRNA. However, the role of FLT3 in cerebral I/R injury was rarely investigated. Real-time polymerase chain reaction revealed that FTL3 expression was negatively regulated by miR-455-5p. FTL3 upregulation reversed the inhibitory effects of miR-455-5p upregulation on PC-12 and SH-SY5Y cell apoptosis. Therefore, our study verified that miR-455-5p improved cerebral I/R injury by targeting FLT3, which suggests a potential new target for the prevention of cerebral I/R injury.Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. Long noncoding RNAs have demonstrated to be associated with AMI pathogenesis. In this study, we aimed to investigate the function and mechanism of zinc finger antisense 1 (ZFAS1) on hypoxia/reoxygenation (H/R)-induced injury in HL-1 cells. The levels of ZFAS1, miR-761, and cell death-inducing p53 target 1 (CDIP1) in the serum of AMI patients and HL-1 cells were detected by quantitative real-time polymerase chain reaction or western blot. Cell viability and apoptosis were assessed by the Cell Counting Kit-8 assay and flow cytometry, respectively. Lactate dehydrogenase release, malondialdehyde content, superoxide dismutase expression, and glutathione peroxidase were evaluated using commercially corresponding assay kits. Targeted interactions among ZFAS1, miR-761, and CDIP1 were validated by dual-luciferase reporter and RNA immunoprecipitation assays. https://www.selleckchem.com/products/luzindole.html Our data indicated that ZFAS1 was upregulated and miR-761 was downregulated in the serum of patients with AMI and H/R-induced HL-1 cells. ZFAS1 silencing or miR-761 overexpression alleviated H/R-induced injury in HL-1 cells. Moreover, ZFAS1 acted as a sponge to sequester miR-761, and CDIP1 was directly targeted and inhibited by miR-761. ZFAS1 knockdown protected HL-1 cell from H/R-induced injury through miR-761, and CDIP1 mediated the alleviated effect of miR-761 overexpression on H/R-induced HL-1 cell injury. Furthermore, ZFAS1 regulated CDIP1 expression through acting as a miR-761 sponge. In addition, CDIP1 silencing protected HL-1 cell from H/R-induced injury. Our current work suggested that the knockdown of ZFAS1 protected against H/R-induced injury in HL-1 cells at least partly through the regulation of miR-761/CDIP1 axis, illuminating a novel therapeutic avenue for AMI management.Long noncoding RNA taurine-upregulated gene 1 (TUG1) has been reported to involve in the processing of cardiac ischemia/reperfusion injury after myocardial infarction. Thus, this study further investigates the underlying mechanisms of TUG1 in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury in vitro.
Cell viability, apoptosis, and migration and invasion were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, and transwell assay, respectively. Western blot was used to examine the levels of matrix metallopeptidase 9, matrix metallopeptidase 2, and sex determining region Y-box transcription factor 8 (Sox8) protein. Levels of lactate dehydrogenase, malondialdehyde, superoxide dismutase, and glutathione peroxidase were detected using commercial kits. Levels of TUG1, microRNA-532-5p (miR-532-5p), and Sox8 were detected by quantitative real-time polymerase chain reaction. The interaction between miR-532-5p and Sox8 or TUG1 was confirmed by dual-luciferase rrdial ischemia/reperfusion injury.Atherosclerosis (AS) is a cardiovascular disease caused by multiple factors, leading to high mortality and morbidity in aged people. Some long noncoding RNAs have been reported to be associated with AS progression. However, the roles of OIP5-AS1 in AS development are still little known. In this study, the levels of OIP5-AS1 and miR-26a-5p in oxidized low-density lipoprotein (ox-LDL)-treated human umbilical vein endothelial cells (HUVECs) were determined by quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were evaluated by Cell Counting Kit-8 assay and flow cytometric analysis, respectively. The protein levels of proliferating cell nuclear antigen, B-cell lymphoma-2, cleaved caspase 3, inflammatory cytokines (IL-6 and IL-1β), protein kinase B (AKT), p-AKT, p65, p-p65, IκBα, and p-IκBα were detected by Western blot analysis. The targeting relationship between OIP5-AS1 and miR-26a-5p was verified by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. As a result, the expression of OIP5-AS1 was upregulated and miR-26a-5p was downregulated in ox-LDL-treated HUVECs. MiR-26a-5p was identified as a direct target of OIP5-AS1. OIP5-AS1 knockdown reversed the inhibitory effect on cell proliferation and the promotional effects on apoptosis and inflammation induced by ox-LDL treatment in HUVECs. Interestingly, the effects caused by OIP5-AS1 knockdown were further attenuated by miR-26a-5p inhibition. Furthermore, OIP5-AS1 knockdown blocked the AKT/NF-κB pathway by regulating miR-26a-5p expression. In conclusion, OIP5-AS1 knockdown promoted cell proliferation and suppressed apoptosis and inflammatory response in ox-LDL-treated HUVECs by targeting miR-26a-5p through blocking the AKT/NF-κB pathway, indicating a promising strategy for AS treatment.